3 Infection

The reservoir of trypanosomes are humans, cattle and antelopes. Carriers of the sleeping sickness are diurnal biting houseflies (tsetse fly). They are endemic to tropical Africa, predominantly in wetlands (rivers, swamps), but also in dry savannahs (e.g. Kalahari). Its sting is very painful and can occur even through fabric. The protozoa enter the bite lesion with the flyâ€™s saliva. The saliva primarily inhibits the coagulation processes. One bite can transmit several thousand protozoa. Theoretically, one single trypansome is enough to trigger the disease.

4 Infection risk

Not all tsetse flies are trypanosome vectors, so not every bite inevitably leads to an infection. The rate of endemic infection varies widely regionally and is given as 1:100 to 1:1000. The risk thereby increases proportionally to the number of bites. The infection predominantly affects the indigenous population. Tourists are mainly at risk, if they stay for a longer period in the endemic area.

5 Epidemiology

The incidence pattern of the sleeping sickness is difficult to ascertain regionally; the disease occurs in Africaâ€™s entire tropical region. According to WHO estimates, more than 500,000 humans are affected by trypanosomiasis. Due to the volatile political situation in many regions (refugees), the rate of the disease has increased in recent years.

6 Pathology

The course of the disease depends on the triggering protist. In an infection with trypanosomea brucei gambiense, the course of the disease is slower, and in an infection with trypanosomea brucei rhodesiense, it is as a rule faster and more pronounced.

Stage I (hemolymphatic phase): In the first week after the infection, a painful swelling with a central vesicle, the so-called "trypanosomal chancre," can occur on the bite. This symptom however appears only in 5-20% of the infected people. One to three weeks after the infection, the actual parasitemia sets in, accompanied by fever, ague, pain in the head and limbs, edema, itching, exanthem and swelling of the lymphatic nodes. Additional symptoms are anemia and thrombocytopenia, as well as elevated IgM levels.

Stage II (meningoencephalitic phase): Approx. 4-6 months after infection - in T.b. rhodiense often already after a few weeks - the protozoa invade the CNS. The patients suffer from increasing states of confusion, reduced coordination and sleeping disorders, seizures, apathy and weight loss. There can be extrapyramidal disorders or a clinical picture similar to that of Parkinsonâ€™s disease. In the final stage, the patients fall into continuous slumber, which is how the disease received its named. The cerebrospinal fluid shows pleocytosis. The disease is lethal after a course of months or years.

7 Immune response

The trypanosomes are surrounded by glycoproteins, the so-called "variable surface glycoproteins" (VSGs). The VSGs are regularly varied by the protozoa during reproduction to escape the immune response of the host (antigenic variation). In the trypanosome genome, more than 1000 different VSG genes are coded, which are alternatively expressed. Even though the human immune system can produce antibodies against the prevalent antigenes, it can only eliminate part of the protist, since new variants already circulate in the blood.

8 Diagnostics

In stage I, the protozoa can be detected microscopically in the blood ("thick drop") or by biopsy of the lymphatic nodes. If the pathology corresponds to stage II, the cerebrospinal fluid is additionally examined. Immunodiagnostic procedures include ELISA, IFT and PHA.

9 Prophylaxis

At present (2004), there exists no medicinal prophylaxis for sleeping sickness. The only option is the avoidance of bites. Tourists should protect themselves with repellents, mosquito nets and long-sleeved clothes. However, these measures are successful only to a limited extent, since tsetse flies are very aggressive, and there are always unprotected areas on the body.

10 Therapy

Due to the toxicity of available medicines, sleeping sickness is treated in most cases in the hospital. In stage II, arsenic compounds are given that trigger pronounced side effects. Lethality may be up to 5%.

Stage I: Administration of suramin (T. b. rhodesiense) or pentamidine (T. b. gambiense). Both medicines do not affect protists in the CNS, since they do not pass the blood-brain barrier.